Hippocampus/Memory Flashcards
explicit memory
“that”
- true/false
- involves modeling of external world
- storage of facts/episodes
- highly flexible; many components
implicit memroy
“how”
- not propositional (procedural)
- change in skilled behavior
- not conscious- motor learning
explicit memory is broken down into
episodic–memory of personal experience
semantic– words/concepts
structures involved in formation of explicit memory
hippocampus proper
dentate gyrus
subiculum
entorhinal cortex
R hippocampus
spatial information
L hippocampus
objects
4 phases of explicit memory
1) encoding– new info is attended to and linked to existing information
2) storage- mechanism/actual brain parts of memory retention
3) consolidation- temporary to permanent
4) retrieval- recall
medial temporal lobe
foramtion of new memories, but stored elsewhere
short term/working memory
PFC
two components
- verbal information
-visuospatial information
efficacy can be changed by
modulating neurons in PFC
- ACH on muscarinic receptors–>change Ca2+ act on nonselective cation channels
- act D1 dopamine R: working memory best when in intermediate range
long term potentiation involves
functional changes in -# post syn R - post syn R channel fx - presyn NT release structural changes in - # post syn spines (new synapses vs elim) - size os spine heads - spine stability
perfornat pathway
axons from entor cells–>granule cells ind entate gyrus–>pyramidal cells CA3 of hippocampus (mossy fiber pathway) GLUTAMATE–>pyramidal neurons of CA1 (schaffer collaterals)–>back to entorinal/subiculum
neurophysiolo postulate
following a high level of presyn activation, the size of synaptic field potentials (epsp amplitudes) in CA1 post syn neurons are larger than they were before and response remains long after presyn activity decreases
damage to place cells
cannot do water maze
LTP characterized by
- induction (bchemical process that arise from high levels of activation)
- expression (long term structural and functional changes)
to induce LTP
presyn high lvel activity
post syn must depol
act on AMPA and NMDA
influx Ca into cell
at rest
low levels of glutamate bind AMPA R–>small depolarization
glutamate binds NMDA R–> no current because Mg2+ binds channel
high levels presyn activity
more glutamate–>act AMPA R–>large depol (-40mv)–>Mg2+ repelled from NMDA R–>positive ion flow into cell–greater depolarization
NMDA therefore acts as a
coincidence detector
pharm blockers or deletion (cre/lox) inhibit LTP
Ca into cell
activates a set of kinases (PKA, PKC, CAMKII)
1) inserts new AMPA R from vesicles at spine head
2) phos AMPAR (stabilizes, greater ion flux increases sensitivity)
3) dynamic restructing of actin cytoskeletion (enlargement, new spines)
4) increasd release of glut from presyn cel
(NO synthase–phos by CAMKII–>makes NO–>locally diffuse to presyn terminal
BDNF
places a role in postsyn ampa r insertion
ltp does/does not req gene expression
DOES
CAMKII, PKA, PKC act downstream to change gene transcription
epigenetics
kinase phos KREB–>interacts with CBP –>histone acetylation–>restructures chromatin
fear
enhanced meth of BDNF gene–>inhibits BDNF expression–>impairs hippocamp role in contextual fear memory
purpse of LTD
erase imporatance of previously held memories in stressful situations so can focus on whats at hand
stress
hippocampal neurons-->express both classical and gCC R and membrane gCC R-->changes kinase signaling increases glut (therefore increases AMPA R) increase LTD, dec LTP ->paradoxical, but resest threshold of lTP when something new need to be learned?
